Changes in the expression of NO synthase isoforms after ozone: the effects of allergen exposure

Jang, An‐Soo; Choi, In Suck; Lee, Jong-Un; Park, Sung Woo; Lee, June-Hyuk; Park, Choon-Sik

doi:10.1186/1465-9921-5-5

Cited by 15 publications

(12 citation statements)

References 26 publications

(19 reference statements)

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“…Jang and colleagues have previously demonstrated nNOS expression in the lung after ozone exposure, but not after allergen exposure, and it is interesting that this was accompanied by a reduction in iNOS expression, consistent with our findings in patients with COPD (29). Higher levels of oxidative and nitrative stress are seen in patients with COPD (21) and we now report an increase in nNOS expression.…”

Section: Choosesupporting

confidence: 92%

“…Jang and colleagues demonstrated that eNOS and nNOS isoforms induce airway responsiveness in mice after ozone exposure, whereas iNOS is decreased, suggesting that eNOS and nNOS contribute to the formation of NO metabolites in mice after ozone exposure (29,41). Grasemann and colleagues investigated the existence of a genetic association between a polymorphism in the nNOS gene and the diagnosis of asthma, concluding that nNOS may be a candidate gene for asthma (42).…”

Section: Choosementioning

confidence: 99%

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Nitric Oxide Synthase Isoenzyme Expression and Activity in Peripheral Lung Tissue of Patients with Chronic Obstructive Pulmonary Disease

Brindicci

Kharitonov²,

Ito³

et al. 2010

Am J Respir Crit Care Med

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Rationale: Nitric oxide (NO) is increased in the lung periphery of patients with chronic obstructive pulmonary disease (COPD). However, expression of the NO synthase(s) responsible for elevated NO has not been identified in the peripheral lung tissue of patients with COPD of varying severity. Objectives:Methods: Protein and mRNA expression of nitric oxide synthase type I (neuronal NOS [nNOS]), type II (inducible NOS [iNOS]), and type III (endothelial NOS [eNOS]) were quantified by Western blotting and reverse transcription-polymerase chain reaction, respectively, in specimens of surgically resected lung tissue from nonsmoker control subjects, patients with COPD of varying severity, and smokers without COPD, and in a lung epithelial cell line (A549). The effects of nitrative/oxidative stress on NOS expression and activity were also evaluated in vitro in A549 cells. nNOS nitration was quantified by immunoprecipitation and dimerization of nNOS was detected by low-temperature SDS-PAGE/Western blot in the presence of the peroxynitrite generator, 3-morpholinosydnonimine-N-ethylcarbamide (SIN1), in vitro and in vivo. Measurements and Main Results:Lung tissue from patients with severe and very severe COPD had graded increases in nNOS (mRNA and protein) compared with nonsmokers and normal smokers. Hydrogen peroxide (H 2 O 2 ) and SIN1 as well as the cytokine mixture (IFN-γ, IL-1β, and tumor necrosis factor-α) increased mRNA expression and activity of nNOS in A549 cells in a concentration-dependent manner compared with nontreated cells. Tyrosine nitration resulted in an increase in nNOS activity in vitro, but did not affect its dimerization. Conclusions:Patients with COPD have a significant increase in nNOS expression and activity that reflects the severity of the disease and may be secondary to oxidative stress.

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Section: Choosesupporting

confidence: 92%

Section: Choosementioning

confidence: 99%

Nitric Oxide Synthase Isoenzyme Expression and Activity in Peripheral Lung Tissue of Patients with Chronic Obstructive Pulmonary Disease

Brindicci

Kharitonov²,

Ito³

et al. 2010

Am J Respir Crit Care Med

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“…In this study, Arginase I expression was found in airway smooth muscles in smokers but not in non-smokers. Among ambient air pollutants, exposure to high levels of ozone has been also been shown to produce oxidative stress and inflammation which can modulate NOS isoform expressions 16. Therefore, it is plausible that the mechanism for the variation of the association of ARG1 and ARG2 variants with asthma in children with different ambient air pollutant exposures (e.g., ozone, PM 2.5 , etc) could be in part due to differences in arginase isoform expression.…”

Section: Introductionmentioning

confidence: 99%

Roles of arginase variants, atopy, and ozone in childhood asthma

Salam¹,

Islam²,

Gauderman³

et al. 2009

Journal of Allergy and Clinical Immunology

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“…We demonstrated that concentrations of NO metabolites increased with asthma severity in the tracheo-bronchial secretions of asthmatic subjects, and that NO metabolites in sputum are a more valuable indicator for monitoring asthmatic airway inflammation than those in serum . The nitric oxide synthase (NOS) isoforms play different roles in airway inflammation after ozone exposure (Jang et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Ym1 and Ym2 expression in a mouse model exposed to diesel exhaust particles

Song

Jang

Ahn

et al. 2008

Environmental Toxicology

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Background: Chitinase may play a role in regulating allergic diseases. Objective: We studied the role of chitinase in a mouse model exposed to diesel exhaust particles (DEP). Mice were exposed to intranasal DEP (0.6 mg/mL) for 5 days and challenged with aerosolized DEP (6 mg/m 3 ) on days 6-8. Enhanced pause (Penh), as an airway obstruction marker, was measured on day 9, and bronchoalveolar lavage (BAL) fluid and lung tissues were collected on day 10. The expression of Ym1 and Ym2 mRNA was assessed in lung tissue extracts by reverse transcription-polymerase chain reaction. Results: DEP induced significant increases in methacholine-induced Penh and IL-4 levels in BAL fluid relative to the control group. Peribronchial and perivascular inflammatory cell infiltrates were prominent in the DEP group. DEP induced Ym1 and Ym2 mRNA expression in lung tissue extracts relative to the control group.-Conclusion: These results demonstrate that DEP induced airway hyperresponsiveness and Ym mRNA expression via a Th2 cell-biased response, suggesting that chitinase may play an important role in airway inflammation and responsiveness upon exposure to DEP in a mouse model, and may therefore be involved in regulating allergic diseases. #

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Changes in the expression of NO synthase isoforms after ozone: the effects of allergen exposure

Abstract: Background: The functional role of nitric oxide (NO) and various nitric oxide synthase (NOS) isoforms in asthma remains unclear.

Cited by 15 publications

References 26 publications

Nitric Oxide Synthase Isoenzyme Expression and Activity in Peripheral Lung Tissue of Patients with Chronic Obstructive Pulmonary Disease

Nitric Oxide Synthase Isoenzyme Expression and Activity in Peripheral Lung Tissue of Patients with Chronic Obstructive Pulmonary Disease

Roles of arginase variants, atopy, and ozone in childhood asthma

Ym1 and Ym2 expression in a mouse model exposed to diesel exhaust particles

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